Sodium selenite has alleviating effects on liver fibrosis; however, its therapeutic molecular mechanism remains unclear. Herein, hydrogen selenide, a major metabolite of NaSeO, was tested to uncouple the sulfilimine bond in collagen IV, the biomarker of liver fibrosis. A mouse model of liver fibrosis was constructed via a CCl-induced method, followed by the administration of 0.2 mg kg NaSeO via gavage three times per week for 4 weeks. Changes in HSe, NADPH, and HO levels were monitored in real time by using NIR-HSe, DCI-MQ-NADPH, and HO probes in vivo, respectively. HSe continuously accumulated in the liver throughout the NaSeO treatment period, but the levels of NADPH and HO decreased. The expression of collagen IV was analyzed through Western blot and liquid chromatography-mass spectrometry. Results confirmed that the sulfilimine bond of collagen IV in the fibrotic mouse livers could be broken by HSe with the NaSeO treatment. Therefore, the therapeutic effect of NaSeO on liver fibrosis could be mainly attributed to HSe that uncoupled the sulfilimine bond to induce collagen IV degradation. This study provided a reasonable explanation for the molecular mechanism of the in vivo function of NaSeO and the prevention of liver fibrosis by administering inorganic selenium.
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